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Aging and disease    2015, Vol. 6 Issue (5) : 400-405     DOI: 10.14336/AD.2015.0617
Review Article |
Potential Therapeutical Contributions of the Endocannabinoid System towards Aging and Alzheimer’s Disease
Amandine E. Bonnet1, Yannick Marchalant2,*()
1 CNRS, NICN UMR 7259 Aix-Marseille University, 13344 Marseille, France.
2 Department of Psychology/Neuroscience program, Central Michigan University, MI 48859, USA
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Aging can lead to decline in cognition, notably due to neurodegenerative processes overwhelming the brain over time. As people live longer, numerous concerns are rightfully raised toward long-term slowly incapacitating diseases with no cure, such as Alzheimer’s disease. Since the early 2000’s, the role of neuroinflammation has been scrutinized for its potential role in the development of diverse neurodegenerative diseases notably because of its slow onset and chronic nature in aging. Despite the lack of success yet, treatment of chronic neuroinflammation could help alleviate process implicated in neurodegenerative disease. A growing number of studies including our own have aimed at the endocannabinoid system and unfolded unique effects of this system on neuroinflammation, neurogenesis and hallmarks of Alzheimer’s disease and made it a reasonable target in the context of normal and pathological brain aging.

Keywords Cannabinoids      Neuroinflammation      Neurogenesis      Aging      Alzheimer’s disease     
Corresponding Authors: Yannick Marchalant     E-mail:
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present address: Kunming Biomed International, Kunming, Yunnan, 650500, China

Issue Date: 01 October 2015
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Amandine E. Bonnet
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Amandine E. Bonnet,Yannick Marchalant. Potential Therapeutical Contributions of the Endocannabinoid System towards Aging and Alzheimer’s Disease[J]. Aging and disease, 2015, 6(5): 400-405.
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[1] Walsh DM, Selkoe DJ (2004). Deciphering the molecular basis of memory failure in Alzheimer’s disease. Neuron, 44(1):181-93.
[2] Akiyama H, Barger S, Barnum S, Bradt B, Bauer J, Cole GM,et al. (2000). Inflammation and Alzheimer’s disease. Neurobiol Aging, 21(3):383-421.
[3] Laferla FM, Green KN, Oddo S (2007). Alzheimer’s disease, 8(July):499-509.
[4] Walsh DM, Selkoe DJ. (2007). A beta oligomers - a decade of discovery. J Neurochem. 101(5):1172-84.
[5] Kuret J, Chirita CN, Congdon EE, Kannanayakal T, Li G, Necula M,et al. (2005). Pathways of tau fibrillization. Biochim Biophys Acta, 1739(2-3):167-78.
[6] Haass C, Selkoe DJ (2007). Soluble protein oligomers in neurodegeneration: lessons from the Alzheimer’s amyloid beta-peptide. Nat Rev Mol Cell Biol, 8(2):101-12.
[7] Ballatore C, Lee VM-Y, Trojanowski JQ (2007). Tau-mediated neurodegeneration in Alzheimer’s disease and related disorders. Nat Rev Neurosci, 8(9):663-72.
[8] Herrup K (2010). Reimagining Alzheimer’s Disease--An Age-Based Hypothesis. J Neurosci, 30(50):16755-62.
[9] Glass CK, Saijo K, Winner B, Marchetto MC, Gage FH. (2010). Mechanisms underlying inflammation in neurodegeneration. Cell. 140(6):918-34.
[10] McGeer PL, Yasojima K, McGeer EG (2002). Association of interleukin-1 beta polymorphisms with idiopathic Parkinson’s disease. Neurosci Lett, 326(1):67-9.
[11] McGeer PL (2001). COX-2 and ALS. Amyotroph Lateral Scler Other Motor Neuron Disord, 2(3):121-2.
[12] McGeer PL, Schulzer M, McGeer EG (1996). Arthritis and anti-inflammatory agents as possible protective factors for Alzheimer’s disease: a review of 17 epidemiologic studies. Neurology, 47(2):425-32.
[13] Vlad SC, Miller DR, Kowall NW, Felson DT (2008). Protective effects of NSAIDs on the development of Alzheimer disease. Neurology, 70(19):1672-7.
[14] Stewart WF, Kawas C, Corrada M, Metter EJ (1997). Risk of Alzheimer’s disease and duration of NSAID use. Neurology, 48(3):626-32.
[15] Griffin WS, Sheng JG, Royston MC, Gentleman SM, McKenzie JE, Graham DI,et al. (1998). Glial-neuronal interactions in Alzheimer’s disease: the potential role of a “cytokine cycle” in disease progression. Brain Pathol, 8(1):65-72.
[16] McGeer PL, Akiyama H, Kawamata T, Yamada T, Walker DG, Ishii T (1992). Immunohistochemical localization of beta-amyloid precursor protein sequences in Alzheimer and normal brain tissue by light and electron microscopy. J Neurosci Res, 31(3):428-42.
[17] Heneka MT, O’Banion MK (2007). Inflammatory processes in Alzheimer’s disease. J Neuroimmunol, 184(1-2):69-91.
[18] Giri R, Selvaraj S, Miller CA, Hofman F, Yan SD, Stern D,et al. (2002). Effect of endothelial cell polarity on beta-amyloid-induced migration of monocytes across normal and AD endothelium. Am J Physiol Cell Physiol, 283(3):C895-904.
[19] Fuller S, Münch G, Steele M (2009). Activated astrocytes: a therapeutic target in Alzheimer’s disease? Expert Rev Neurother, 9(11):1585-94.
[20] Wu Q, Combs C, Cannady SB, Geldmacher DS, Herrup K (2000). Beta-amyloid activated microglia induce cell cycling and cell death in cultured cortical neurons. Neurobiol Aging, 21(6):797-806.
[21] Wyss-Coray T (2006). Inflammation in Alzheimer disease: driving force, bystander or beneficial response? Nat Med, 12(9):1005-15.
[22] Chakrabarty P, Li A, Ceballos-Diaz C, Eddy JA, Funk CC, Moore B,et al. (2015), IL-10 alters immunoproteostasis in APP mice, increasing plaque burden and worsening cognitive behavior. Neuron, 85(3):519-33.
[23] Schmidt R, Schmidt H, Curb JD, Masaki K, White LR, Launer LJ (2002). Early inflammation and dementia: a 25-year follow-up of the Honolulu-Asia Aging Study. Ann Neurol, 52(2):168-74.
[24] Engelhart MJ, Geerlings MI, Meijer J, Kiliaan A, Ruitenberg A, van Swieten JC,et al. (2004). Inflammatory proteins in plasma and the risk of dementia: the rotterdam study. Arch Neurol, 61(5):668-72.
[25] Dunn N, Mullee M, Perry VH, Holmes C (2005). Association between dementia and infectious disease: evidence from a case-control study. Alzheimer Dis Assoc Disord, 19(2):91-4.
[26] Aisen PS, Schafer KA, Grundman M, Pfeiffer E, Sano M, Davis KL,et al. (2003). Effects of rofecoxib or naproxen vs placebo on Alzheimer disease progression: a randomized controlled trial. JAMA, 289(21):2819-26.
[27] Thal LJ, Ferris SH, Kirby L, Block GA, Lines CR, Yuen E,et al. (2005). A randomized, double-blind, study of rofecoxib in patients with mild cognitive impairment. Neuropsychopharmacology, 30(6):1204-15.
[28] Breitner JC, Baker LD, Montine TJ, Meinert CL, Lyketsos CG, Ashe KH,et al. (2011). Extended results of the Alzheimer’s disease anti-inflammatory prevention trial. Alzheimers Dement, 7(4):402-11.
[29] Crystal H, Dickson D, Fuld P, Masur D, Scott R, Mehler M,et al. (1988). Clinico-pathologic studies in dementia: nondemented subjects with pathologically confirmed Alzheimer’s disease. Neurology, 38(11):1682-7.
[30] Lue LF, Brachova L, Civin WH, Rogers J (1996). Inflammation, A beta deposition, and neurofibrillary tangle formation as correlates of Alzheimer’s disease neurodegeneration. J Neuropathol Exp Neurol, 55(10):1083-8.
[31] Schwab C, Hosokawa M, McGeer PL (2004). Transgenic mice overexpressing amyloid beta protein are an incomplete model of Alzheimer disease. Exp Neurol, 188(1):52-64.
[32] Cagnin A, Brooks DJ, Kennedy AM, Gunn RN, Myers R, Turkheimer FE,et al. (2001). In-vivo measurement of activated microglia in dementia. Lancet, 358(9280):461-7.
[33] Yokokura M, Mori N, Yagi S, Yoshikawa E, Kikuchi M, Yoshihara Y,et al. (2011). In vivo changes in microglial activation and amyloid deposits in brain regions with hypometabolism in Alzheimer’s disease. Eur J Nucl Med Mol Imaging, 38(2):343-51.
[34] Lee CYD, Landreth GE. (2010). The role of microglia in amyloid clearance from the AD brain. J Neural Transm, 117(8):949-60.
[35] Grathwohl SA, Kälin RE, Bolmont T, Prokop S, Winkelmann G, Kaeser SA,et al. (2009). Formation and maintenance of Alzheimer’s disease beta-amyloid plaques in the absence of microglia. Nat Neurosci, 12(11):1361-3.
[36] Sheng JG, Mrak RE, Griffin WS (1997). Neuritic plaque evolution in Alzheimer’s disease is accompanied by transition of activated microglia from primed to enlarged to phagocytic forms. Acta Neuropathol, 94(1):1-5.
[37] Streit WJ (2006). Microglial senescence: does the brain’s immune system have an expiration date? Trends Neurosci, 29(9):506-10.
[38] Krstic D, Madhusudan A, Doehner J, Vogel P, Notter T, Imhof C,et al. (2012). Systemic immune challenges trigger and drive Alzheimer-like neuropathology in mice. J Neuroinflammation, 9(1):151.
[39] Matsuda LA, Lolait SJ, Brownstein MJ, Young AC, Bonner TI (1990). Structure of a cannabinoid receptor and functional expression of the cloned cDNA. Nature, 346(6284):561-4.
[40] Munro S, Thomas KL, Abu-Shaar M (1993). Molecular characterization of a peripheral receptor for cannabinoids. Nature, 365(6441):61-5.
[41] Pertwee RG (2010). Receptors and channels targeted by synthetic cannabinoid receptor agonists and antagonists. Curr Med Chem, 17(14):1360-81.
[42] Herkenham M, Groen BG, Lynn AB, De Costa BR, Richfield EK (1991). Neuronal localization of cannabinoid receptors and second messengers in mutant mouse cerebellum. Brain Res, 552(2):301-10.
[43] Núñez E, Benito C, Pazos MR, Barbachano A, Fajardo O, González S,et al. (2004). Cannabinoid CB2 receptors are expressed by perivascular microglial cells in the human brain: an immunohistochemical study. Synapse, 53(4):208-13.
[44] Van Sickle MD, Duncan M, Kingsley PJ, Mouihate A, Urbani P, Mackie K,et al. (2005). Identification and functional characterization of brainstem cannabinoid CB2 receptors. Science. 310(5746):329-32.
[45] Ashton JC, Friberg D, Darlington CL, Smith PF. (2006). Expression of the cannabinoid CB2 receptor in the rat cerebellum: an immunohistochemical study. Neurosci Lett. 396(2):113-6.
[46] Bisogno T, Ligresti A, Di Marzo V. (2005). The endocannabinoid signalling system: biochemical aspects. Pharmacol Biochem Behav. 81(2):224-38.
[47] Piomelli D. (2003). The molecular logic of endocannabinoid signalling. Nat Rev Neurosci. 4(11):873-84.
[48] Vaughan CW, Christie MJ. (2005). Retrograde signalling by endocannabinoids. Handb Exp Pharmacol. (168):367-83.
[49] Klein TW (2005). Cannabinoid-based drugs as anti-inflammatory therapeutics. Nat Rev Immunol, 5(5):400-11.
[50] Prentiss D, Power R, Balmas G, Tzuang G, Israelski DM (2004). Patterns of marijuana use among patients with HIV/AIDS followed in a public health care setting. J Acquir Immune Defic Syndr, 35(1):38-45.
[51] Walsh D, Nelson KA, Mahmoud FA (2003). Established and potential therapeutic applications of cannabinoids in oncology. Support Care Cancer, 11(3):137-43.
[52] Maresz K, Pryce G, Ponomarev ED, Marsicano G, Croxford JL, Shriver LP,et al. (2007). Direct suppression of CNS autoimmune inflammation via the cannabinoid receptor CB1 on neurons and CB2 on autoreactive T cells. Nat Med, 13(4):492-7.
[53] Eljaschewitsch E, Witting A, Mawrin C, Lee T, Schmidt PM, Wolf S,et al. (2006). The endocannabinoid anandamide protects neurons during CNS inflammation by induction of MKP-1 in microglial cells. Neuron, 49(1):67-79.
[54] Marchalant Y, Cerbai F, Brothers HM, Wenk GL (2008). Cannabinoid receptor stimulation is anti-inflammatory and improves memory in old rats. Neurobiol Aging, 29(12):1894-901.
[55] Marchalant Y, Brothers HM, Wenk GL (2009). Cannabinoid agonist WIN-55,212-2 partially restores neurogenesis in the aged rat brain. Mol Psychiatry, 14(12):1068-9.
[56] Marchalant Y, Brothers HM, Norman GJ, Karelina K, DeVries a. C, Wenk GL (2009). Cannabinoids attenuate the effects of aging upon neuroinflammation and neurogenesis. Neurobiol Dis, 34(2):300-7.
[57] Marchalant Y, Rosi S, Wenk GL (2007). Anti-inflammatory property of the cannabinoid agonist WIN-55212-2 in a rodent model of chronic brain inflammation. Neuroscience, 144(4):1516-22.
[58] Ramírez BG, Blázquez C, Gómez del Pulgar T, Guzmán M, de Ceballos ML (2005). Prevention of Alzheimer’s disease pathology by cannabinoids: neuroprotection mediated by blockade of microglial activation. J Neurosci, 25(8):1904-13.
[59] Solas M, Francis PT, Franco R, Ramirez MJ (2013). CB2 receptor and amyloid pathology in frontal cortex of Alzheimer’s disease patients. Neurobiol Aging, 34(3):805-8.
[60] Benito C, Núñez E, Tolón RM, Carrier EJ, Rábano A, Hillard CJ,et al. (2003). Cannabinoid CB2 receptors and fatty acid amide hydrolase are selectively overexpressed in neuritic plaque-associated glia in Alzheimer’s disease brains. J Neurosci, 23(35):11136-41.
[61] Lee JH, Agacinski G, Williams JH, Wilcock GK, Esiri MM, Francis PT,et al. (2010). Intact cannabinoid CB1 receptors in the Alzheimer’s disease cortex. Neurochem Int, 57(8):985-9.
[62] Mulder J, Zilberter M, Pasquaré SJ, Alpár A, Schulte G, Ferreira SG,et al. (2011). Molecular reorganization of endocannabinoid signalling in Alzheimer’s disease. Brain, 134(Pt 4):1041-60.
[63] Ahmad R, Goffin K, Van den Stock J, De Winter F-L, Cleeren E, Bormans G,et al. (2014). In vivo type 1 cannabinoid receptor availability in Alzheimer’s disease. Eur Neuropsychopharmacol, 24(2):242-50.
[64] Milton NGN (2002). Anandamide and noladin ether prevent neurotoxicity of the human amyloid-beta peptide. Neurosci Lett, 332(2):127-30.
[65] Chen X, Zhang J, Chen C (2011). Endocannabinoid 2-arachidonoylglycerol protects neurons against β-amyloid insults. Neuroscience, 178:159-68.
[66] Harvey BS, Ohlsson KS, Mååg JL V, Musgrave IF, Smid SD (2012). Contrasting protective effects of cannabinoids against oxidative stress and amyloid-β evoked neurotoxicity in vitro. Neurotoxicology, 33(1):138-46.
[67] Janefjord E, Mååg JL V, Harvey BS, Smid SD (2014). Cannabinoid effects on β amyloid fibril and aggregate formation, neuronal and microglial-activated neurotoxicity in vitro. Cell Mol Neurobiol, 34(1):31-42.
[68] Esposito G, De Filippis D, Steardo L, Scuderi C, Savani C, Cuomo V,et al. (2006). CB1 receptor selective activation inhibits beta-amyloid-induced iNOS protein expression in C6 cells and subsequently blunts tau protein hyperphosphorylation in co-cultured neurons. Neurosci Lett, 404(3):342-6.
[69] Sciences ML, Stelt M Van Der, Mazzola C, Esposito G, Matias I, Petrosino S,et al. (2006). Endocannabinoids and β -amyloid-induced neurotoxicity in vivo : effect of pharmacological elevation of endocannabinoid levels, 63:1410-24.
[70] Haghani M, Janahmadi M, Shabani M (2011). Protective effect of cannabinoid CB1 receptor activation against altered intrinsic repetitive firing properties induced by Aβ neurotoxicity. Neurosci Lett, 507(1):33-7.
[71] Wu J, Bie B, Yang H, Xu JJ, Brown DL, Naguib M (2013). Activation of the CB2 receptor system reverses amyloid-induced memory deficiency. Neurobiol Aging, 34(3):791-804.
[72] Martín-Moreno AM, Reigada D, Ramírez BG, Mechoulam R, Innamorato N, Cuadrado A,et al. (2011). Cannabidiol and other cannabinoids reduce microglial activation in vitro and in vivo: relevance to Alzheimer’s disease. Mol Pharmacol, 79(6):964-73.
[73] Fakhfouri G, Ahmadiani A, Rahimian R, Grolla AA, Moradi F, Haeri A (2012). WIN55212-2 attenuates amyloid-beta-induced neuroinflammation in rats through activation of cannabinoid receptors and PPAR-γ pathway. Neuropharmacology, 63(4):653-66.
[74] Aso E, Palomer E, Juvés S, Maldonado R, Muñoz FJ, Ferrer I (2012). CB1 agonist ACEA protects neurons and reduces the cognitive impairment of AβPP/PS1 mice. J Alzheimers Dis, 30(2):439-59.
[75] Aso E, Juvés S, Maldonado R, Ferrer I (2013). CB2 cannabinoid receptor agonist ameliorates Alzheimer-like phenotype in AβPP/PS1 mice. J Alzheimers Dis, 35(4):847-58.
[76] Martín-Moreno AM, Brera B, Spuch C, Carro E, García-García L, Delgado M,et al. (2012). Prolonged oral cannabinoid administration prevents neuroinflammation, lowers β-amyloid levels and improves cognitive performance in Tg APP 2576 mice. J Neuroinflammation, 9:8.
[77] Marchalant Y, Rosi S, Wenk GL (2007). Anti-inflammatory property of the cannabinoid agonist WIN-55212-2 in a rodent model of chronic brain inflammation. Neuroscience, 144(4):1516-22.
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